Masked inherited primary arrhythmia syndromes in sudden cardiac death patients accompanied by coronary vasospasm.

BACKGROUND/AIMS: Coronary vasospasms are one of the important causes of sudden cardiac death (SCD). Provocation of coronary vasospasms can be useful, though some results may lead to false positives, with patients potentially experiencing recurrent SCD despite appropriate medical treatments. We hypothesized that it is not coronary vasospasms but inherited primary arrhythmia syndromes (IPAS) that underlie the development of SCD. METHODS: We analyzed 74 consecutive patients (3.8%) who survived out-of-hospital cardiac arrest among 1,986 patients who had angiographically proven coronary vasospasms. Electrical abnormalities were evaluated in serial follow-up electrocardiograms (ECGs) during and after the index event for a 3.9 years median follow-up. Major clinical events were defined as the composite of death and recurrent SCD events. RESULTS: Forty five patients (60.8%) displayed electrocardiographic abnormalities suggesting IPAS: Brugada type patterns in six (8.2%), arrhythmogenic right ventricular dysplasia patterns in three (4.1%), long QT syndrome pattern in one (2.2%), and early repolarization in 38 (51.4%). Patients having major clinical events showed more frequent Brugada type patterns, early repolarization, and more diffuse multivessel coronary vasospasms. Brugada type pattern ECGs (adjusted hazard ratio [HR], 4.22; 95% confidence interval [CI], 1.16 to 15.99; p = 0.034), and early repolarization (HR, 2.97; 95% CI, 1.09 to 8.10; p = 0.034) were ultimately associated with an increased risk of mortality. CONCLUSIONS: Even though a number of aborted SCD survivors have coronary vasospasms, some also have IPAS, which has the potential to cause SCD. Therefore, meticulous evaluations and follow-ups for IPAS are required in those patients.

Clinical outcome prediction from mean platelet volume in patients undergoing percutaneous coronary intervention in Korean cohort: Implications of more simple and useful test than platelet function testing.

The aim of this study was to determine the associations of the mean platelet volume (MPV) with the development of adverse outcomes after percutaneous coronary intervention (PCI) and platelet reactivity. MPV and platelet function testing were analysed in 208 patients who underwent PCI. The primary endpoint was cardiac death. The secondary endpoint analysed was cardiovascular events (CVE): the composite of myocardial infarction (MI), target vessel revascularization (TVR), and stent thrombosis (ST). The median MPV level, aspirin reaction unit (ARU), P2Y12 reaction units (PRU) and P2Y12% inhibition (PI%) of clopidogrel were 8.55 (IQR 8.00-9.18) fl, 401.0 (IQR 389.3-442.0) ARU, 222.0 (IQR 169.0-272.3) PRU and 22 (IQR 9-38) %, respectively. We observed that high values of MPV were associated with elevated ARU (r = 0.165, p = 0.017) and decreased PI% (r = -0.167, p = 0.016). There were 10 events of cardiac death, 3 MI (including 1 event of ST), and 8 TVR during a mean of 7.6 months of follow-up. The Kaplan-Meier analysis revealed that the higher MPV group (≥8.55 fl, median) had a significantly higher cardiac death rate compared to the lower MPV group (<8.55 fl) (7.7% vs. 1.9%, log-rank: p = 0.035). However, aspirin or clopidogrel resistance (>550 ARU, <40 PI%, respectively) did not predict cardiac death. When the MPV cut-off level was set to 8.55 fl using the receiver operating characteristic curve, the sensitivity was 80% and the specificity was 51.5% for differentiating between the group with cardiac death and the group without cardiac death. This value was more useful in patients with clinical diagnosis of acute coronary syndrome (ACS). Furthermore, ACS patients with an MPV over 8.55 fl had high cardiac death and CVE risk without atorvastatin loading before PCI (Log-Rank = 0.0031, 0.0023, respectively). The results of this study show that MPV was a predictive marker for cardiac death after PCI; its predictive power for cardiac death was more useful in patients with ACS.

An optimal cardiothoracic ratio cut-off to predict clinical outcomes in patients with acute myocardial infarction.

The traditional cut-off for the cardiothoracic ratio (CTR) by chest X-ray was not originally proposed as a prognostic variable. We investigated an optimal CTR cut-off that could predict clinical outcomes in patients with acute myocardial infarction (AMI). A total of 3,083 AMI patients (65.2 ± 12.0 years, 2,091 males) who underwent successful percutaneous coronary intervention were divided into two groups by use of a CTR of 0.42 as determined by receiver-operating characteristic curve analysis (group I: CTR ≤ 0.42, group II: CTR > 0.42). We compared the incidences of in-hospital death and major adverse cardiac events (MACEs), including cardiac death, reinfarction, coronary artery bypass grafting, and target lesion revascularization, during 12 months between the groups. The patients in group II were older than those in group I and included more women. The patients in group II were more likely to have hypertension and multivessel disease and had a higher Killip class, higher troponin, higher N-terminal pro-brain natriuretic peptide, and lower ejection fraction than did those in group I. The in-hospital death rate was higher in group II (1.9 vs. 4.8%, p < 0.001). The incidences of cardiac death and composite of MACEs during 12 months of follow-up were significantly higher in group II than in group I (2.4 vs. 5.7%, p < 0.001, and 16.0 vs. 19.8%, p = 0.007, respectively). Multivariable logistic regression analysis revealed that CTR greater than 0.42 was an independent predictor of MACEs (relative risk: 1.361, 95% CI 1.014-1.827, p = 0.040). A CTR greater than 0.42, although within the traditional normal range, was associated with worse in-hospital and long-term clinical outcome in AMI patients.

Relation of triiodothyronine to subclinical myocardial injury in patients with chest pain.

Heart dysfunctions have been shown to be associated with altered concentrations of thyroid hormones. However, the relation between thyroid hormones and subclinical myocardial injury in those without clinically apparent coronary heart disease is not well-established. We examined the correlation between altered levels of thyrotropin, free thyroxine, and triiodothyronine (T3) and high-sensitivity cardiac troponin T (hs-cTnT) in 250 patients (mean age 60 years; 42% men) with chest pain, who were free of coronary heart disease and heart failure. These patients were examined in the emergency room or outpatient department of the cardiovascular center of Chosun University Hospital. Multivariate logistic regression models were used for statistical analysis. The baseline values of T3 were associated with elevated hs-cTnT levels (r = -0.428, p <0.001), a significantly negative correlation. We did not observe any significant correlation between the thyrotropin or free thyroxine and hs-cTnT levels. When the T3 cutoff was set at 74.6 ng/dl using the receiver operating characteristic curve, the sensitivity and specificity was 70% and 69%, respectively, for differentiating between groups with and without myocardial injury. After adjusting for traditional risk factors, the odds ratio for an elevated hs-cTnT level (≥0.014 ng/ml) for patients with T3 <74.6 ng/dl was 6.95 (95% confidence interval 3.09 to 15.66) compared to patients with T3 ≥74.6 ng/dl. In conclusion, the T3 levels were negatively related to hs-cTnT levels among patients without clinically obvious coronary heart disease.